Pulmonary embolism: a treatable cause of cardiac arrest?

Abstract

Pulmonary embolism is a major cause of morbidity and mortality throughout the world. This disorder complicates such common illnesses as malignancy, heart failure, and stroke, and is associated with surgical procedures and immobility. More recently, inherited disorders of the clotting cascade have been identified that increase the risk of forming venous thromboses. However, even with these advances in knowledge, pulmonary embolism remains a common cause of unexpected death (1). This situation is unlikely to improve. Most patients with pulmonary embolism have underlying chronic diseases (2), the incidence of which is increasing with lifeprolonging technologies and the aging of the population. Also, a growing number of critically ill patients who are immobilized with intravenous catheters have been documented with venous thrombosis and pulmonary embolism (3). The stakes are high in diagnosing pulmonary embolism, because the therapy is highly effective. When pulmonary embolism is correctly diagnosed and treated, the risk of death from this disorder is less than 3% in the first year (2). Untreated, the mortality from pulmonary embolism may be as great as 30%. Unfortunately, the diagnosis of pulmonary embolism is challenging, because its signs and symptoms can be confused with such common conditions as congestive heart failure, pneumonia, or coronary heart disease. Consequently, there has been a longstanding quest to discover the ideal way to diagnose pulmonary embolism. Technologies have included radionuclide imaging of the lung, selective angiography of the pulmonary circulation, and most recently, high-resolution and spiral computerized tomographic (CT) scanning of the lung. Each of these techniques is imperfect, with limitations ranging from accuracy (lung scan and CT) to cost and complexity (angiography). Therefore, combining noninvasive technologies, such as lung scan and venous ultrasound of the lower extremities, has been favored as a way to document venous clots. One of the most dramatic and ominous symptoms of pulmonary embolism is syncope, often caused by a large venous clot that temporarily obstructs the right ventricular outflow tract. Even without syncope, a large pulmonary clot burden increases pulmonary vascular resistance and results in right ventricular dilation and strain. When studied by echocardiography, this phenomenon may be more common than previously realized (4). In critically ill patients suspected of pulmonary embolism, echocardiography can reveal clots in the right heart chambers or main pulmonary arteries, or new right ventricular dilation suggesting pulmonary embolus (5). In this issue of The Green Journal, Comess et al (6) have used these observations to study patients presenting with unexplained cardiac arrest and pulseless electrical activity. The question was whether pulmonary embolism is a major cause of this clinical condition. For diagnosis, the investigators used transesophageal echocardiography, which improves visualization of right heart clots compared with the standard transthoracic technique. Using conventional and blinded echo interpretations, Comess et al found that 9 of 35 cardiac arrest victims (36%) with pulseless electrical activity had pulmonary embolism. All but 1 of these patients was diagnosed by transesophageal echocardiography. This report thus adds to a growing literature suggesting that echocardiography should join the armamentarium of noninvasive techniques for diagnosing pulmonary embolism (7). This simple, widely available technology is particularly helpful in seriously ill patients in whom a large clot burden is suspected. The second implication of this report, which should be viewed more cautiously, is that pulmonary embolism is a common diagnosis in cardiac arrest. During the study period of 3 years, there were 481 patients with cardiac arrest, of whom only 36 entered the study. Therefore, as the authors point out, their study has considerable selection bias. The studied patients must have survived to be resuscitated, had sustained pulseless electrical activity, had no clear cause for cardiac arrest, and had a physician who requested transesophageal echocardiography. Therefore, this study cannot determine the true prevalence of pulmonary embolism in patients with cardiac arrest. A recent report, also using transesophageal echocardiography for diagnosis, suggested that pulmonary embolism occurs in approximately 5% of patients who have cardiac arrest, but this study was retrospective (8). Thus, we have no definitive answers. Am J Med. 2000;109:427– 428. From the Henry Ford Medical Group, Detroit, Michigan. Requests for reprints should be addressed to Mark A. Kelley, MD, the Henry Ford Health System, One Ford Place, Detroit, Michigan 48202.